Introduction
A 5-year-old spayed female domestic shorthair cat was presented to a local emergency hospital for evaluation of an acute onset of dyspnea and open-mouthed breathing. The patient had a 3-day history of lethargy and inappetence. Prior to this time, the cat did not have any notable medical problems and had not been receiving heartworm prophylaxis. The patient was a lifelong indoor-only cat and was the only pet in the household.
Physical examination revealed pink to cyanotic mucous membranes with a normal capillary refill time, dyspnea, intermittent open-mouthed breathing, and tachypnea (respiratory rate, 60 breaths/min). Thoracic auscultation revealed muffled heart sounds, tachycardia (heart rate, 176 beats/min), and crackles in the cranioventral lung fields. Focused thoracic ultrasonography revealed mild to moderate pleural effusion. Results of a CBC and serum biochemical analyses, including measurement of total thyroxine concentration, were within reference limits; results of tests for heartworm antigen, FeLV antigen, and anti-FIV antibody were negative; and results of a test for N-terminal pro–B-type natriuretic peptide were positive. Supplemental oxygen was provided (40% inspired oxygen), and the patient was administered butorphanol (0.15 mg/kg, IV) and furosemide (2 mg/kg, IV).
Therapeutic thoracocentesis was performed, and the obtained fluid was white, suggestive of chylothorax. Thoracic radiography revealed pleural effusion, diffuse regions of increased soft tissue opacity concentrated in the caudodorsal lung lobes, atelectasis of the cranial lung lobes, mild pneumothorax, and rounded lung margins consistent with restrictive pleuritis. The cat remained hospitalized for 34 hours, receiving ampicillin-sulbactam (30 mg/kg, IV, q 8 h), enrofloxacin (5 mg/kg, IV, q 24 h), and supplemental oxygen (40% inspired oxygen). Furosemide administration was discontinued because congestive heart failure was considered unlikely. The cat rapidly became dyspneic and tachypneic when the inspired oxygen concentration was decreased from 40%; therefore, the cat was transferred to a tertiary-care referral hospital for further diagnostic testing and treatment.
On presentation at our hospital, the cat’s physical examination findings were unchanged. Packed cell volume, total solids concentration, and results of point-of-care testing for electrolyte concentrations and renal function (iSTAT; Abbott Point of Care) were consistent with mild dehydration. Thoracic radiography was repeated, revealing progressive pleural effusion, but no other changes from previous images were apparent. Abnormalities on repeated CBC and serum biochemistry analyses consisted of lymphopenia (585 cells/µL; reference range, 850 to 5,850 cells/μL), thrombocytopenia (90,000 platelets/µL; reference range, 155,000 to 641,000 platelets/µL), hypochloremia (105 mmol/L; reference range, 114 to 126 mmol/L]), high bicarbonate concentration (33 mmol/L; reference range, 12 to 22 mmol/L), hypertriglyceridemia (109 mg/dL; reference range, 20 to 90 mg/dL), and high creatine kinase activity (976 U/L; reference range, 64 to 440 U/L). There was a notation of platelet clumping; however, subsequent platelet evaluation by manual review of the slides did not reveal any abnormalities.
Echocardiography revealed normal cardiac size, structure, and function with mild pulmonary hypertension suspected to be secondary to pulmonary disease. The cat was hospitalized in an oxygen cage set to deliver 40% inspired oxygen. While results of further diagnostic testing were pending, the cat was treated empirically with ampicillin-sulbactam (30 mg/kg, IV, q 8 h) and enrofloxacin (5 mg/kg, IV, q 24 h). Overnight, the cat remained tachypneic but did not appear dyspneic.
On day 2 of hospitalization, CT was performed. The patient was premedicated with butorphanol (0.4 mg/kg, IV), and anesthesia was induced with propofol (0.81 mg/kg, IV) and maintained with constant rate infusions of propofol (0.1 to 0.2 mg/kg/min, IV) and butorphanol (0.1 to 0.2 mg/kg/min, IV). Oxygen was provided through an endotracheal tube. A review of the CT images revealed diffuse, severe restrictive pleuritis, bilateral, moderate pleural effusion, and multifocal pulmonary atelectasis. There was no evidence of pulmonary nodules or an identifiable cause for the pleural effusion.
Thoracocentesis was performed as previously described,1,2 which yielded a red, turbid fluid. Analysis of the fluid revealed a protein concentration of 4.6 g/dL, an RBC count of 150,000 RBCs/µL, a mixed leukocyte population (40% macrophages, 47% nondegenerate neutrophils, and 13% small lymphocytes), a high triglyceride concentration (326 mg/dL; reference range, 20 to 90 mg/dL), and a low cholesterol concentration (58 mg/dL; reference range, 91 to 305 mg/dL). Findings were consistent with a diagnosis of chylous effusion with chronic inflammation. No infectious agents or neoplastic cells were identified. A platelet count was performed, and prothrombin and partial thromboplastin times were measured; results were within reference limits. Antimicrobial treatment was discontinued, but supportive fluid therapy and oxygen supplementation (40% inspired oxygen via an oxygen cage) were continued. Because the patient’s oxygen dependency and tachypnea had not improved with supportive care and antimicrobial treatment, surgery to relieve the restrictive pleuritis was considered the only remaining treatment option.
Surgery was performed on day 4 of hospitalization. The patient was premedicated with maropitant (1 mg/kg, IV), morphine (0.48 mg/kg, IV), dexmedetomidine (1.9 µg/kg, IV), and ondansetron (0.30 mg/kg, IV). General anesthesia was induced with a combination of midazolam (0.48 mg/kg, IV) and ketamine (3.21 mg/kg, IV) and maintained with a constant rate infusion of ketamine (1.2 mg/kg/h, IV) and inhalant sevoflurane.
Owing to the extensive, bilateral nature of the cat’s restrictive pleuritis, a median sternotomy was performed to maximize visualization of and access to both hemithoraces. There were diffuse adhesions throughout both hemithoraces between the mediastinum, heart, lung lobes, and parietal pleura. Approximately 150 mL of white, opaque, low-viscosity fluid was suctioned from the left hemithorax. Adhesions were debrided with Metzenbaum scissors, cotton-tipped applicators, and a bipolar sealing device (LigaSure Dolphin Tip Open Sealer-Divider; Covidien), until the heart, lung lobes, and mediastinum could be adequately visualized and evaluated.
The pericardium, mediastinum, and lung lobes were each completely encased by an approximately 0.1- to 0.3-cm-thick layer of tan, firm, fibrous tissue (Figure 1). Because of the diffuse adhesions, positive-pressure ventilation failed to inflate any lung lobe to a normal volume, with the cranial and right middle lung lobes most severely affected. Starting at the ventral aspect of the left cranial lung lobe, the enveloping tissue was grasped with an Adson forceps and perforated with mosquito hemostats. A plane was established between the fibrous membrane and visceral pleura, which was separated with dry cotton-tipped applicators (Figure 2). During dissection, iatrogenic tearing of the lung occurred in the left caudal lung lobe and caudal subsegment of the left cranial lung lobe. Closure was achieved with 3-0 polydioxanone in a simple continuous suture pattern (left caudal lung lobe) and with the application of medium hemoclips (caudal subsegment of left cranial lung lobe).
Following complete pleural decortication, lung expansion was markedly and progressively improved, most notably in the caudal lung lobes. Owing to the extent of damage to the cranial subsegment of the left cranial lung lobe, a peripheral lung lobectomy3 was performed with the bipolar sealing device. Subtotal pericardiectomy was subsequently performed with the same device. Owing to the severity of the fibrosis and decreased visualization of the vascular anatomy, thoracic duct ligation was not performed.
The skin incision was extended caudally to include the cranial aspect of the abdomen and allow for omentalization of the thoracic cavity. The omentum was secured to the parietal pleura of the cranial, right and left thoracic walls with 3-0 polydioxanone in a simple interrupted suture pattern. Bilateral 14-gauge, 8-inch thoracostomy tubes (Guidewire-inserted chest tube; MILA International Inc) were placed routinely. The sternum was closed with size-0 polypropylene in a cruciate suture pattern. The overlying musculature was closed with 3-0 polydioxanone in a simple continuous suture pattern, and a 9-inch diffusion catheter (MILA International Inc) was then placed deep to the musculature and affixed to the skin with 3-0 nylon in simple interrupted and finger-trap suture patterns. The linea alba was closed in a simple continuous suture pattern with 3-0 polydioxanone. The subcutaneous and skin layers were closed routinely. The thorax was only partially evacuated to minimize the risk of reexpansion pulmonary edema.4,5,6
Postoperative treatments included ampicillin-sulbactam (22 mg/kg, IV, q 8 h), methadone (0.2 mg/kg, IV, q 6 h), ketamine (0.3 mg/kg/h, IV as a constant rate infusion), intermittent local infusion of bupivacaine (0.5 mg/kg, q 4 to 6 hours) through the diffusion catheter, and nebulization with saline (0.45% NaCl) solution (q 6 h). Oxygen supplementation was tapered so long as the cat maintained a normal oxygen saturation as measured by pulse oximetry (Spo2) and normal respiratory effort.
The cat remained hospitalized for 7 days after surgery. Thoracic radiography 2 days after surgery revealed improved pulmonary expansion, most notably in the right cranial and middle lung lobes. Pleural effusion progressively decreased, with the left thoracostomy tube removed on day 2, and the right thoracostomy tube removed on day 7. The cat was transitioned from methadone to buprenorphine (0.02 mg/kg, IV, q 8 h) 1 day after surgery, and buprenorphine administration was discontinued on day 6. The constant rate infusion of ketamine was discontinued on day 2, and the diffusion catheter was removed on day 3. Dexamethasone (0.5 mg/kg, IV, q 12 h) was added to the treatment regimen on day 3, which was transitioned to oral prednisolone administration on day 5.
Oxygen supplementation was maintained with an inspired oxygen fraction of 40% to 60% for the first 3 days after surgery. An increased respiratory effort and supplemental oxygen dependency persisted initially; however, the cat improved daily throughout the hospitalization period, although it remained tachypneic. The cat was progressively weaned off oxygen supplementation starting on day 3. By day 5, the inspired oxygen fraction had been reduced to approximately 25%, and the cat was weaned off oxygen supplementation entirely on day 6.
The cat was discharged 7 days after surgery with a prescription for amoxicillin–clavulanic acid (14 mg/kg, PO, q 12 h) to be administered for 5 days. The owner was advised to administer prednisolone (0.5 mg/kg, PO, q 12 h) and rutin (250 mg, PO, q 8 h) for the rest of the cat’s life and to transition the cat to a low-calorie diet (Feline Metabolic Diet; Hill’s Pet Nutrition) or a low-calorie, high-fiber diet (Feline w/d; Hill’s Pet Nutrition). Tapering the dosage of prednisolone was to be considered on the basis of clinical signs and adverse effects. However, as of the last follow-up, the dosage of prednisolone had not been adjusted because the cat was doing well clinically without any adverse effects associated with prednisolone administration.
Results of histologic examination of the pericardium and fibrous membrane fragments were consistent with severe pleural fibrosis secondary to chronic chylothorax, with moderate lymphoplasmacytic and mildly eosinophilic fibrinous pleuritis. No fungal or bacterial pathogens or neoplastic processes were identified.
One week after discharge, the client reported that the cat was doing well at home, was very energetic, and had a normal respiratory effort but remained tachypneic. Follow-up examinations were performed 3, 7, and 20 weeks after surgery. The cat continued to receive prednisolone (0.5 mg/kg, PO, q 12 h), rutin (50 mg/kg, PO, q 8 h), and a low-calorie diet. On examination, the cat was consistently tachypneic but had a normal respiratory effort, and vital parameters were otherwise normal. Focused thoracic ultrasonography performed at each examination revealed progressively improved pleural effusion. By week 20, there was trace pleural effusion in the right hemithorax and no pleural effusion in the left hemithorax. Radiography performed at each examination revealed consistently improved lung volume expansion and progressively decreased pleural effusion; pneumothorax had resolved by week 20 (Figure 3).
Discussion
Fibrosing pleuritis secondary to chronic chylothorax carries a grave prognosis with limited treatment options.2,7,8,9,10 Medical management of chylothorax is commonly pursued initially, because the condition can spontaneously resolve.11 Options for medical management include the use of rutin (50 to 100 mg/kg, PO, q 8 h)2,12,13 and corticosteroids, feeding a low triglyceride diet, and therapeutic thoracocentesis as needed to resolve dyspnea.13,14 If clinical signs are recognized in the chronic stages, such as in this case, or medical or surgical management fails to correct the chylothorax, pleural thickening occurs and fibrous adhesions form between the parietal and visceral lung pleura, which restrict lung expansion.2,7,8,9,10 Clinical signs can remain mild for months, and recognition of associated lethargy, dyspnea, or tachypnea by owners is often discordant with the disease timeline. Thus, owners often report an acute onset of clinical signs.2,10,11
Surgical intervention is indicated in cats and dogs with chylothorax if medical management has failed or disease chronicity has progressed to such a degree that medical management alone is no longer successful.12 Prior to pursuing surgery, diagnostic imaging, heartworm antigen testing, and a cardiac evaluation should be used to rule out a primary cause of chylothorax.11,12,15,16 First-line surgical techniques for dogs and cats with chylothorax uncomplicated by severe fibrosing pleuritis include thoracic duct ligation following mesenteric lymphangiography and subtotal pericardiectomy.2,15,16 Additionally, pleural omentalization has shown fair to good clinical outcomes.2,12,17,18,19 Open or thoracoscopic en bloc thoracic duct ligation may also be considered as a first-line technique when combined with subtotal pericardiectomy because it has the benefit of short surgical time, since lymphangiography is not performed, and showed good clinical success in previous reports.20,21 Additional techniques that can be considered include active or passive pleuroperitoneal shunting, pleurovenous shunting, pleurodesis, and cisterna chyli ablation, either with or without thoracic duct glue embolization, but are not recommended as first-line treatments.12,22,23,24 Despite the many techniques available, all of these surgical options fail to improve lung volume expansion once fibrosing pleuritis has developed.13,25
Prior to surgery and intraoperatively, lymph node injection of new methylene blue to improve thoracic duct visualization, en bloc thoracic duct ligation, vascular access port placement, and thoracic omentalization were all considered for the cat described in the present report.11,12,14,17,22,26 Owing to the severity of the pleuritis encountered during surgery, long anesthetic time, and severely altered anatomy, thoracic omentalization was ultimately elected. Additionally, the patient had been positioned in dorsal recumbency for the median sternotomy to improve visualization of the lungs, so open en bloc thoracic duct ligation was not pursued because this procedure has previously been performed in cats in lateral recumbency.20 This procedure, however, was considered for the future if needed to address recurrent chylothorax in this patient.
A pericardiectomy was performed in this patient to reduce the risk of chylothorax recurrence. Pericardiectomy as part of a multilevel surgical approach to idiopathic chylothorax has improved patient outcomes in previous reports,11,12,14,21 with the proposed mechanism involving normalizing lymph flow through the thoracic duct as a result of decreased systemic venous pressure. Additionally, because of the severe, diffuse pleuritis in this patient, pericardiectomy was specifically pursued to reduce the risk for subsequent development of restrictive cardiomyopathy.
Previous attempts at pleural decortication in animals with restrictive pleuritis have resulted in poor outcomes, with patients being euthanized because of marked reexpansion pulmonary edema and failure to resolve respiratory distress.10,11,14,27 Glennon et al27 performed decortication in an 18-year-old cat, and in that case, continuous suction was used postoperatively (suction rate was not reported) and resulted in life threatening reexpansion pulmonary edema, which led to euthanasia. Stewart and Padgett14 reported outcomes of cats with > 50% fibrosing pleuritis treated with pleural decortication, en bloc thoracic duct ligation, subtotal pericardiectomy, and thoracic omentalization. Two of 3 cats in which decortication was performed died in the immediate postoperative period (2 and 4 days postoperatively) owing to aortic thrombosis, an acute onset of dyspnea, and respiratory arrest. LaFond et al17 described omentalization for treatment of idiopathic chylothorax in a cat in which restrictive pleuritis was seen at the time of surgery. Decortication was attempted but limited to 25% because of difficulties associated with separating the fibrous adhesions. An estimated 50% increase in pulmonary expansion was noted, despite the limited decortication that was performed. Thoracic duct ligation was not performed owing to an inability to safely visualize the thoracic duct during surgery and a historically low rate of successful treatment in cats.15,16,17 The cat eventually made a full recovery.
In light of a previous report14 of patients developing postoperative thrombosis, thorough screening preoperatively for clotting abnormalities via prothrombin time, partial thromboplastin time, and platelet count and for cardiac disease via echocardiography; blood pressure monitoring; and monitoring an ECG along with correction of any metabolic abnormalities, especially those that can predispose to a hypercoagulable state, may be prudent.
The success of this case described in the present report, compared with outcomes in previous reports, may have been due to vital differences in patient health and surgical and postoperative management. Similar to what was observed by LaFond et al,17 the cat described in this report was young to middle age and free from cardiac and metabolic comorbidities. In an attempt to limit the risk of reexpansion pulmonary edema, the cat’s thorax was incompletely evacuated via the thoracostomy tubes.28,29 Thoracocentesis was performed to the point that Spo2 was normal, and the cat’s tachypnea improved without achieving negative pressure. Continuous suction was not used postoperatively, in contrast to the report by Glennon et al,27 who used continuous postoperative suction in an 18-year-old cat with underlying hyperthyroidism and cardiac disease that subsequently developed reexpansion pulmonary edema. The poor outcome for that cat may not have been due to the surgical technique, but rather to the cat’s underlying health problems and the postoperative management. Additionally, in the report by Stewart and Padgett,14 2 of 4 cats died postoperatively because of aortic thromboembolism and acute respiratory distress. The extent to which cats in that study were preoperatively screened for underlying cardiac and metabolic diseases and coagulopathies was not discussed.
The extent of restrictive pleuritis described by LaFond et al17 in their report was less severe than in the cat described in the present report, which may have been why incomplete decortication and unilateral thoracic omentalization were successful. Decortication was not limited by difficulty separating the fibrosed pleura in the present case, so complete decortication could be performed. These differences bring into question the extent to which decortication should be performed on the basis of the percentage of lung affected.
In human medicine, open thoracotomy and pleural decortication is the standard of care for symptomatic patients with restrictive pleuritis secondary to chylothorax, empyema, or pseudochylothorax.30,31,32 Surgical success is superior to that published in veterinary medicine, with mortality rates of 0% to 8%.33 Reexpansion pulmonary edema is a rare complication seen in human patients undergoing treatment for pneumothorax or pleural effusion drainage, but still has a mortality rate ranging from 5% to 20%.6,34,35 The pathogenesis in humans is still not fully understood, but factors that increase the risk of developing reexpansion pulmonary edema include greater duration of atelectasis, increased pulmonary vascular permeability, rapid pulmonary expansion, and the use of negative pressure to reexpand the lung. Studies have also shown reexpansion pulmonary edema to occur independently of these factors.6,34,35
Future investigation into the extent to which pleural decortication should be performed in patients with restrictive pleuritis and into the optimal postoperative management regimen to reduce the risk of thromboembolism and reexpansion pulmonary edema is warranted. Studies are also needed of the extent to which additional procedures, such as pericardiectomy and thoracic duct ligation, improve clinical outcomes.
To our knowledge, the present case represented the first successful report of complete decortication being used to treat restrictive pleuritis in a cat. Although clients should still be made aware that the surgery itself and postoperative recovery have been associated with life-threatening risks, we have shown that surgical intervention can be pursued in cats with restrictive pleuritis cases and can result in good, long-term outcomes.
References
- 1. ↑
Sturgess K. Diagnosis and management of chylothorax in dogs and cats. In Pract. 2001;23(9):506–513.
- 2. ↑
Fossum TW. Section V: cardiology and respiratory disorders. In: August JR, ed. Consultations in Feline Internal Medicine. 5th ed. Elsevier; 2006:369–375.
- 3. ↑
Mayhew PD, Culp WTN, Pascoe PJ, Vapniasky Arzi N. Use of the Ligasure vessel-sealing device for thoracoscopic peripheral lung biopsy in healthy dogs. Vet Surg. 2012;41(4):523–528.
- 4. ↑
Stampley AR, Waldron DR. Reexpansion pulmonary edema after surgery to repair a diaphragmatic hernia in a cat. J Am Vet Med Assoc. 1993;203(12):1699–1701.
- 5. ↑
Melis SM, de Rooster H, Waelbers T, Polis I. Anesthesia Case of the Month. J Am Vet Med Assoc. 2014;245(11):1230–1234.
- 6. ↑
Mahfood S, Hix WR, Aaron BL, Blaes P, Watson DC. Reexpansion pulmonary edema. Ann Thorac Surg. 1988;45(3):340–345.
- 7. ↑
Thompson MD, Carr AP. Hyponatremia and hyperkalemia associated with chylous pleural and peritoneal effusion in a cat. Can Vet J. 2002;43(8):610–613.
- 9. ↑
Willauer CC, Breznock EM. Pleurovenous shunting technique for treatment of chylothorax in three dogs. J Am Vet Med Assoc. 1987;191(9):1106–1109.
- 10. ↑
Fossum TW, Evering WN, Miller MW, Forrester SD, Palmer DR, Hodges CC. Severe bilateral fibrosing pleuritis associated with chronic chylothorax in five cats and two dogs. J Am Vet Med Assoc. 1992;201(2):317–324.
- 11. ↑
Fossum TW, Mertens MM, Miller MW, et al.. Thoracic duct ligation and pericardectomy for treatment of idiopathic chylothorax. J Vet Intern Med. 2004;18(3):307–310.
- 12. ↑
Fossum TW. Chylothorax in cats: is there a role for surgery? J Feline Med Surg. 2001;3(2):73–79.
- 13. ↑
Thompson MS, Cohn LA, Jordan RC. Use of rutin for medical management of idiopathic chylothorax in four cats. J Am Vet Med Assoc. 1999;215(3):345–8, 339.
- 14. ↑
Stewart K, Padgett S. Chylothorax treated via thoracic duct ligation and omentalization. J Am Anim Hosp Assoc. 2010;46(5):312–317.
- 15. ↑
Fossum TW, Forrester SD, Swenson CL, et al.. Chylothorax in cats: 37 cases (1969–1989). J Am Vet Med Assoc. 1991;198(4):672–678.
- 16. ↑
Kerpsack SJ, McLoughlin MA, Birchard SJ, Smeak DD, Biller DS. Evaluation of mesenteric lymphangiography and thoracic duct ligation in cats with chylothorax: 19 cases (1987–1992). J Am Vet Med Assoc. 1994;205(5):711–715.
- 17. ↑
LaFond E, Weirich WE, Salisbury SK. Omentalization of the thorax for treatment of idiopathic chylothorax with constrictive pleuritis in a cat. J Am Anim Hosp Assoc. 2002;38(1):74–78.
- 18. ↑
Talavera J, Agut A, del Palacio JF, Martínez CM, Seva JI. Thoracic omentalization for long-term management of neoplastic pleural effusion in a cat. J Am Vet Med Assoc. 2009;234(10):1299–1302.
- 19. ↑
Williams JM, Niles JD. Use of omentum as a physiologic drain for treatment of chylothorax in a dog. Vet Surg. 1999;28(1):61–65.
- 20. ↑
Bussadori R, Provera A, Martano M, et al.. Pleural omentalisation with en bloc ligation of the thoracic duct and pericardiectomy for idiopathic chylothorax in nine dogs and four cats. Vet J. 2011;188(2):234–236. doi: 10.1016/j.tvjl.2010.05.010
- 21. ↑
Haimel G, Liehmann L, Dupré G. Thoracoscopic en bloc thoracic duct sealing and partial pericardectomy for the treatment of chylothorax in two cats. J Feline Med Surg. 2012;14(12):928–931.
- 22. ↑
Brooks AC, Hardie RJ. Use of the PleuralPort device for management of pleural effusion in six dogs and four cats. Vet Surg. 2011;40(8):935–941. doi: 10.1111/j.1532-950X.2011.00901.x
- 23. ↑
Clendaniel DC, Weisse C, Culp WTN, Berent A, Solomon JA. Salvage cisterna chyli and thoracic duct glue embolization in 2 dogs with recurrent idiopathic chylothorax. J Vet Intern Med. 2014;28(2):672–677.
- 24. ↑
Stockdale SL, Gazzola KM, Strouse JB, Stanley BJ, Hauptman JG, Mison MB. Comparison of thoracic duct ligation plus subphrenic pericardiectomy with or without cisterna chyli ablation for treatment of idiopathic chylothorax in cats. J Am Vet Med Assoc. 2018;252(8):976–981.
- 25. ↑
Greenberg MJ, Weisse CW. Spontaneous resolution of iatrogenic chylothorax in a cat. J Am Vet Med Assoc. 2005;226(10):1667–1670.
- 26. ↑
Enwiller TM, Radlinsky MG, Mason DE, Roush JK. Popliteal and mesenteric lymph node injection with methylene blue for coloration of the thoracic duct in dogs. Vet Surg. 2003;32(4):359–364.
- 27. ↑
Glennon JC, Rothwell JT, Flanders JA, et al.. Constrictive pleuritis with chylothorax in a cat: a case report. J Am Anim Hosp Assoc. 1987;23(5):539–543.
- 28. ↑
Macho RG, Worth AJ. Prevention of reexpansion pulmonary edema and ischemia-reperfusion injury in the management of diaphragmatic herniation. Compendium. 2006;28(7):531–540.
- 29. ↑
Worth AJ, Machon RG. Traumatic diaphragmatic herniation: pathophysiology and management. Compendium. 2005;27(3)178–191.
- 30. ↑
Perikleous P, Rathinam S, Waller DA. VATS and open chest surgery in diagnosis and treatment of benign pleural diseases. J Vis Surg. 2017;3:84.
- 31. ↑
Huggins JT. Chylothorax and cholesterol pleural effusion. Semin Respir Crit Care Med. 2010;31(6):743–750.
- 32. ↑
Nair SK, Petko M, Hayward MP. Aetiology and management of chylothorax in adults. Eur J Cardiothorac Surg. 2007;32(2):362–369.
- 33. ↑
Bagheri R, Haghi SZ, Dalouee MN, et al.. Effect of decortication and pleurectomy in chronic empyema patients. Asian Cardiovasc Thorac Ann. 2016;24(3):245–249.
- 35. ↑
Belliraj L, Lakranbi M, Lahlou A, et al.. Acute unilateral reexpansion pulmonary edema after pleuropulmonary decortication. OAJ Case Rep. 2019;1:010. doi: 10.33118/oaj.rep.2019.01.010